929. Genetic diversity of non-O157 Shiga toxin-producing Escherichia coli (STEC) strains associated with disease in Michigan, Connecticut and Utah
Session: Poster Abstract Session: Bacterial Pathogenesis
Saturday, October 22, 2011
Room: Poster Hall B1
Background: An estimated 11,500 to 287,000 foodborne infections are caused by non-O157 STEC each year; this wide range is in part due to the limitations associated with culture-based detection methods.  Unlike O157 STEC, which has been studied extensively, less is known of the genetic diversity and population structure of non-O157 STEC, particularly among strains from geographically distinct patient populations.

Methods: We performed multilocus sequence typing, serotyping, and Shiga toxin (stx) and intimin (eae) gene profiling on 173 non-O157 STEC isolates recovered from patients in Michigan (n=44), Connecticut (n=115), and Utah (n=14) between 2000 and 2006.

Results: Serogroups O26, O45, O103, and O111 predominated, accounting for 132 (76%) of the strains.  Phylogenetic analysis classified the strains into 43 sequence types (STs), which grouped into 13 distinct clonal groups (CGs).  The CGs ranged in size from three to six STs, with the largest CG representing the enterohemorrhagic E. coli (EHEC)-2 lineage.  Overall, STs 78, 104, 106, and 119 predominated (n=125; 72%) and were widespread in that they were detected in all three states over the same time period.  An additional seven STs were found in both Connecticut and Michigan, leaving a total of 36 STs that were unique to one of the three populations.  Interestingly, two STs were comprised of strains with multiple serotypes.  ST-119 of the enteropathogenic (EPEC)-2 CG included serotypes O45:H2 (n=32; 55%) and O103:H2 (n=26; 45%), while ST-106 of EHEC-2 included serotypes O111:H8 (n=26; 55%) and O26:H11 (n=21; 55%).  The stx and eae allele profiles were correlated with STs.  ST-119, for example, had stx1 and eae epsilon alleles most frequently, while ST-106 had stx1 and either eae beta or theta.

Conclusion: Several non-O157 STs are widespread, which is consistent with the hypothesis that some sporadic disease is caused by circulating epidemic clones.   Furthermore, non-O157 STEC of distinct serotypes often belong to the same CG, providing evidence for rapid antigenic shifts in nature.  A better understanding of the genetic diversity of circulating genotypes is important to guide future prevention efforts and identify lineages associated with more severe disease.


Subject Category: B. Bacterial pathogenesis, studies in animal models, molecular pathogenicity

Rebekah Mosci1, Jillian Tietjen1, David Lacher, PhD2, Lindsey Oullette1, Quyen Phan, MPH3, John Fontana, PhD4, Jim Hadler, MD, MPH5, James Rudrik, PhD6 and Shannon Manning, PhD7,8, (1)Michigan State University, East Lansing, MI, (2)U.S. Food and Drug Administration, Silver Spring, MD, (3)CT Dept of Public Health, Hartford, CT, (4)Connecticut Dept. of Public Health, Hartford, CT, (5)Connecticut EIP, Hartford, CT, (6)Michigan Department of Community Health, Lansing, MI, (7)Pediatrics and Human Development, Michigan State University, East Lansing, MI, (8)Michigan State University, E. Lansing, MI

Disclosures:

R. Mosci, None

J. Tietjen, None

D. Lacher, None

L. Oullette, None

Q. Phan, None

J. Fontana, None

J. Hadler, None

J. Rudrik, None

S. Manning, None

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